The objective of this project is to ascertain whether despair behavior in socially separated rhesus monkeys, already established as a behavioral model of some forms of human depression, can also serve as a biochemical-pharmacological model of depression. Alterations in brain catecholamine (CA) metabolism have been implicated as a possible etiological factor in human depression and pharmacological alterations of CA metabolism in monkeys can potentiate or ameliorate despair behavior in a situationally apppropriate context. Initially we intend to determine the degree to which CA metabolism must be compromised before significant social and separation behavioral changes are observed, and then ascertain whether these brain biochemical changes are usefully reflected by changes in urinary or cerebrospinal fluid (CSF) (CA metabolites. These basic studies will provide information about some characteristics of brain CA - behavior interactions and the possibility of using peripherally available biochemical measures as an index of brain function. Further studies using a wide variety of pharmacological agents with relatively well documented behavioral effects in humans, and well documented behavioral and biochemical effects in rodents, will be performed in order to identify important similarities and differences between the behavioral pharmacology of despair in monkeys and depression in humans.